Curing Your Fatty Liver Disease Permanently

The fatty liver remedy is a program that uses natural ways to treat diseases related to fatty liver. The creator of this program goes by the name of Layla Jeffrey and has for the better part of her life majored in the field of nutrition. This program is very secure and safe to use all the recommended methods in the guide because they have undergone testing and results have proven that they give 100% positive results. This program is worth trying as it involves zero-risk. Within 60 days after joining the program, a total money refund is guaranteed to any user who feels unsatisfied with the program. The program is a life changer as it will help you in the elimination of toxic elements in your body, help improve the level of efficiency of your liver. Also, help you save on the cost as you will use natural treatment methods and the program will free bonuses to help boost your health in a big way. Following all the benefits associated with this program, I highly recommend the fatty liver remedy program to everyone as it will enhance your healthy living permanently. Read more here...

The Reduce Your Fatty Liver Program is a digital program designed to help work out the cause of fatty liver disease and what steps to take to reduce its symptoms. Through a variety of resources developed by author Susan Peters, who treated the condition herself when diagnosed with fatty liver disease, readers can reduce the fat build-ups in their livers that could be causing adverse effects to their personal health. As fatty liver disease comes with a host of unpleasant symptoms, such as weight gain, fatigue, skin breakouts, and even long-term liver ailments such as fibrosis or cirrhosis, the program aims to help those suffering from the disease to restore their liver to a natural and healthy condition. Resources included detailed medical information regarding fatty liver disease researched by Susan herself, along with a range of methods to naturally reduce fat in the liver, eliminating the disease entirely and enjoying the benefits of a healthy and functional liver. An in-depth dietary program is also included that aims to deal with the root cause, as poor diet is the leading cause of the condition, while suggestions for supplements, vitamins, minerals, and how to naturally detox the liver are all provided. Read more here...

Reverse Your Fatty Liver Program Summary

The fat content of liver is normally less than 5 of the wet weight. Fatty liver is the condition arising from the progressive infiltration of fat into the liver lobule. Fat content in the liver may increase to 30 of wet weight. Fatty liver is often associated with conditions of undernutrition such as ketosis due to the central role of the liver in the metabolism of fat (Fig. 1). During undernutrition, increased release of NEFA from adipose tissue results in increased uptake of NEFA by liver. In the liver, NEFA can enter the mitochondria for conversion to acetyl CoA and either formation of ketone bodies or complete oxidation. The NEFA that do not enter the mitochondria can be esterified to form phospholipids, cholesterol esters, and triacylglycerols. With adequate glucose availability, CPTI activity is decreased and NEFA are esterified, forming triacylglycerol (TAG). 2 These esterified compounds must be combined with apoproteins and incorporated into very low-density lipoproteins...

There are several advantages to infusing parent-eral nutrition in a cyclic manner over 12-16 h during the hours of sleep. First, it permits the patient to pursue a normal lifestyle during the day hours. Second, it minimizes the risks of fatty liver and hepatomegaly that are associated with long-term continuous calorie and protein infusions.

Although the carcinogenicity of ST is less (10-100 times) than that of AFB1 in test animals (van der Watt 1977), ST is a mutagen and genotoxin and has been found in cereal grains (barley, rice, and corn), coffee beans, and cheese (Chu 2002). A. terreus and several other fungi (e.g., A. flavus and A. fumigatus and some Penicillia) have been found to produce the tremorgenic toxins, territrems, aflatrem, and fumitremorgin. These mycotoxins contain both the indole ring of tryptophan and a dioxopiperazine ring formed by condensation of two amino acids. A. terreus, A. fumigatus, and Trichoderma viride also produce gliotoxin, an epipolythiopiperazines -3,6-diones-sulfur containing piperazine antibiotic, that may have immunosuppressive effects in animals (Waring and Beaver 1996). In addition, A. flavus, A. wentii, A. oryzae, and P. atraovenetum are capable of producing nitropropionic acid (NPA), a mycotoxin causing apnea, convulsions, congestion in lungs and subcutaneous...

Alanine aminotransferase (ALT also called glutamate-pyruvate transaminase, GPT) and aspartate aminotransferase (AST also called glutamate-oxaloacetate transaminase, GOT) are important in the diagnosis of heart and liver damage caused by heart attack, drug toxicity, or infection. After a heart attack, a variety of enzymes, including these aminotransferases, leak from the injured heart cells into the bloodstream. Measurements of the blood serum concentrations of the two aminotransferases by the SGPT and SGOT tests (S for serum) and of another enzyme, creatine kinase, by the SCK test can pro The SGOT and SGPT tests are also important in occupational medicine, to determine whether people exposed to carbon tetrachloride, chloroform, or other industrial solvents have suffered liver damage. Liver degeneration caused by these solvents is accompanied by leakage of various enzymes from injured hepato-cytes into the blood. Aminotransferases are most useful in the monitoring of people exposed to...

Premelanoidins have been shown to inhibit growth, cause liver damage, and interrupt reproduction in laboratory animals. Maillard products of fructose-glycine and fructose-arginine increase the mutagenicity of 3-amino-1,4-dimethyl 5H-pyridol-(4,3-b)indole. Antimutagenic effects seem to correlate well with antioxidant effects. However, mutagenicity of benzo(a)pyrene is moderately inhibited by such products. Some products of the Maillard reaction have been shown to induce allergic reactions.

Hepatic (pertaining to the liver) damage can occur in a number of ways. Fatty liver is an accumulation of lipid globules inside the liver cells and is caused by several Carbon tetrachloride may act in several ways. Besides forming radicals, it can also be converted to phosgene. It also has an indirect effect. It causes a large release of the hormone epinephrine by sympathetic nerves. As with other hormones, epinephrine is quickly broken down after performing its function. This takes place in the liver, and the high levels caused by carbon tetrachloride can result in liver damage. Liver damage can be detected clinically by several functional tests, such as the rate at which it clears certain injected dyes or bilirubin, a chemical produced normally by the breakdown of heme from red blood cells. More sensitive than the liver function tests are tests for certain enzymes. Often when the excretory capability of the liver is impaired, the effects are visible as jaundice, the yellowing of the...

Nielsen et al. (1998a) demonstrated a reduced number of tumour metastases in a murine model of metastatic breast cancer after the intravenous administration of recombinant-adenovirus-expressing p53. This approach, however, resulted in significant liver damage that was thought to be due to the adenoviral vector. New conditionally replicative adenoviral vectors with E1 and E4 gene deletions are much less hepatotoxic and may be useful for p53 transduction in the future.

Symptoms of riboflavin deficiency include a reduction in growth rate, stiffness of gait, alopecia (hair loss), seborrhea (crusty exudates), vomiting, and cataracts. Other deficiency symptoms that have been observed are increased blood neutrophil granulocytes, reduced immune response, discolored kidney and liver tissue, fatty liver, and degeneration of the myelin of the sciatic and brachial nerves. Females with severe deficiency have also been

A long-term study over 101 weeks demonstrated that feeding cats a linoleate-deficient diet resulted in reduced feed efficiency, high rates of transepidermal water loss, poor skin and coat condition, and fatty liver. Supplementation with safflower seed oil, with or without tuna oil, led to prevention of the signs noted above. Further studies reported the pathological changes in various organs after feeding the linoleate-deficient diet, including severe fatty degeneration of

The half-life of caffeine in plasma varies not only with specie differences but also with age and condition of the individual. The half-life in rodent plasma is 1 to 2 h but it is 6 h in that of the healthy adult human. There is variation depending on smoking habits and the use of some medications. During pregnancy the half-life is increased to 18 h. The immature liver of the newborn human is limited in its ability to metabolize caffeine so that its half-life is three to four days, similar to that of adults with severe liver damage. These differences are significant in extrapolating safety data from animal studies and also in considering diet during pregnancy (24).

Alcoholic liver disease The term 'alcoholic liver disease' refers to a spectrum of types of hepatic injury associated with continuous alcohol ingestion, ranging from alcoholic fatty liver to alcoholic stea-tohepatitis, fibrosis, and cirrhosis. Nutritional disturbances in alcoholics are an important cause of morbidity and mortality all classes of nutrients are affected. Anorexia leads to decreased food intake and subsequent protein-calorie malnutrition. Maldigestion and malabsorption can occur secondary to chronic alcohol injury to small intestinal mucosa. Alcohol consumption is often associated with chronic pancreatic insufficiency, which results in steatorrhea and decreased absorption of dietary protein, fat, and fat-soluble vitamins. Chronic alcohol ingestion also results in impaired hepatic amino acid uptake and protein synthesis. A variety of international associations have made nutritional recommendations for patients with various types of alcoholic liver disease. The primary...

SNPs (single nucleotide polymorphisms) in humans may exist and, if so, would influence dietary requirements for choline. In mice in which this gene is knocked out, the dietary requirement for choline is increased and they get fatty liver when eating a normal choline diet. Estrogen induces greater activity of PEMT perhaps explaining why premenopausal women require less choline in their diets. In addition to formation of choline, this enzyme has an essential role in lipoprotein secretion from the liver.

The presence of abdominal pain in nausea and vomiting of pregnancy or hyperemesis gravidarum is highly unusual and should suggest another diagnosis. Occasionally, women with ruptured ectopic pregnancies present with nausea and vomiting as well as diarrhea and abdominal pain. After the first trimester, the volume of the gallbladder increases during fasting and postcontraction after a meal. Also, biliary sludge seems to increase in pregnancy in 30 percent, predisposing to stone formation.7 Cholelithiasis and cholecystitis are more common in pregnant women than in women of comparable age and health status who are not pregnant. Differential diagnosis of vomiting or vomiting with abdominal pain should include cholecystitis, cholelithiasis, gastroenteritis, pancreatitis, hepatitis, peptic ulcer, pyelonephritis, ectopic pregnancy, and fatty liver of pregnancy.

Hepatitis B and C may cause chronic liver damage and due account should be taken of liver function in those patients known to be carriers or known to have had B or C hepatitis. Hepatitis A does not produce chronic sequelae but may present for surgery during the active or prodromal phases of the disease and again, liver function should be tested and the anaesthetic managed accordingly. The AIDS-related conditions may be of interest to the anaesthetist when the patient presents for surgery but the possibilities are so broad that each must be taken on its merits. Patients with PGL may present for lymph node biopsy. Unfortunately, the majority of people infected with hepatitis B, C and HIV are asymptomatic and not known to the medical community. While precautions against cross infection are usually taken in those patients known, to be infected, it is more logical to take precautions in all patients and assume that every patient is potentially infectious. It is thus, wise for anaesthetists...

Alcoholic liver disease is among the top ten causes of mortality in the US with somewhat higher mortality rates in western European countries where wine is considered a dietary staple, and is a leading cause of death in Russia. Among the three stages of alcoholic liver disease, fatty liver is related to the acute effects of alcohol on hepatic lipid metabolism and is completely reversible. By contrast, alcoholic hepatitis usually occurs after a decade or more of chronic drinking, is associated with inflammation of the liver and necrosis of liver cells, and carries about a 40 mortality risk for each hospitalization. Alcoholic cirrhosis represents irreversible scarring of the liver with loss of liver cells, and may be associated with alcoholic hepatitis. The scarring process greatly alters the circulation of blood through the liver and is associated with increased blood pressure in the portal (visceral) circulation and shunting of blood flow away from the liver and through other organs...

This resection threshold may be lower (i.e., even less may be removed) in patients with abnormal liver parenchyma, such as cirrhosis or fatty liver. A clear understanding of liver anatomy is paramount. The hepatectomy can be performed in multiple ways and depends on the anatomy involved with the disease process. Resections can include nonanatomic resections, anatomic segmental resections, anatomic lobe or sectoral resections (left lobe segments II, III, and IV right lobe V, VI, VII, and VIII segment I, the caudate, can be taken with either the left or the right), and complete hepatectomy at the time of transplantation. In order to facilitate the choice of resection, preoperative imaging is mandatory. Once the decision has been made to proceed with resection, some additional staging technique is used in the operating room to assist in the decisions regarding extent of resection and often, to assess resectability in cases of malignancy. These techniques include...

Aldehydes tend to be more irritating than they are CNS depressants. One unique toxicity of the aldehydes, especially formaldehyde, is sensitization. That is, it can increase a person's response to other chemicals. Formaldehyde is a common industrial chemical used in plastics and resins. The LD50 in humans for formalin (37 to 50 formaldehyde solution) is about 45 g, although deaths have been reported at as low as 30 g. Ingestion can produce headaches, GI tract corrosion, pulmonary edema, fatty liver, kidney necrosis, unconsciousness, and vascular collapse. Formaldehyde has been associated with muta-genicity and carcinogenicity in laboratory tests, but a steep dose-response relationship, the lack of epidemiological evidence for carcinogenicity in humans, plus the following facts, suggest the presence of a carcinogenicity threshold. Formaldehyde is a metabolic by-product, normally present at several ppm in tissues. Thus, it appears that carcinogeni-city is associated with exposures high...

Alcoholics have been estimated on average to have a life span 10 to 15 years shorter than that of moderate drinkers or nondrinkers. 4 Increased mortality rates result chiefly from heart and liver disease, cancer, and accidents. Although the occurrence of coronary artery disease is decreased among alcoholics, heavy ethanol use increases the likelihood of hypertension and can cause alcoholic cardiomyopathy. Ethanol is the most common cause of liver failure both in the United States and worldwide. Fatty liver is present in virtually all alcoholics, while 10 to 35 percent develop alcoholic hepatitis. Heavy ethanol use is also associated with increased risk of cancer of the esophagus, stomach, pancreas, liver, and breast.

Of alcohol that would be expected after moderate drinking. The metabolism of alcohol by ADH causes a redox change that promotes lipid synthesis in the liver as well as reduced gluconeogenesis and increased lactate production. Thus, even moderate drinking can cause fatty liver with elevated serum triglyceride levels and, in the absence of dietary carbohydrate, may result in low blood glucose levels that impair concentration and even consciousness. The second liver enzyme, CYP2E1, is part of the cytochrome P450 family, and metabolizes alcohol at levels to be expected after heavy drinking. During metabolism of high levels of alcohol, CYP2E1 utilizes adenosine triphosphate (ATP) energy units and thus 'wastes' stored calories, with resultant potential for weight loss. Another form of this enzyme, gastric CYP2E1, exists in the stomach and, as the first of the three alcohol-metabolizing enzymes to encounter alcohol, accounts for about 30 of all alcohol metabolism in men, but only 10 in...

Tannins have evolved to be less desirable foods for herbivores, and they may protect the plant against microbial and fungal attack. There are two subgroups of tannins the condensed and hydrolyzable compounds (Figure 12.7). Hydrolyzable tannins include gallic, digallic, and ellagic acid esters of glucose or quinic acid. Tannic acid is an example of a hydrolyzable tannin. Condensed tannins are fla-vonoids. They tend to polymerize at positions where carbon bonds link the monomers. Tannins such as gallic acid can tie up metals. Tannins are found in tropical fruits such as mangoes, dates, persimmons, and in tea, coffee, grapes, wine, and cocoa. Black tea contains oxidized tannins. Tannins have been reported to cause liver injury (necrosis and fatty liver). Tannins bind proteins or cause precipitation of proteins, inhibiting digestive enzymes. They also reduce the bioavailability of iron. In the Far East, betel nuts are often chewed after dinner, and because they contain 26 tannins, are...

A reverse tolerance'' has also been described, whereby an alcoholic taking a small quantity of alcohol may become intoxicated, aggressive, and antisocial. This occurs in those who have brain or liver damage and therefore show an enhanced sensitivity to the disinhibiting actions of the drug or a decreased metabolism.

The liver is known to have a very high capacity for regeneration. In fact, mammals (including humans) can survive surgical removal of up to 75 of the total liver mass. The original number of cells is restored within 1 week and the original tissue mass within 2 to 3 weeks. Liver size is also controlled by prevention of organ overgrowth. Hepatic overgrowth can be induced by a variety of compounds such as hepatocyte growth factor (HGF) or peroxisome proliferators, but the liver size returns to normal very rapidly after removal of the growth stimulus. The role of liver stem cells in regeneration has been controversial, but it is now accepted that these cells are important for the repair of specific types of liver damage. In general, however, the cell types and mechanisms responsible for liver repair are determined by the type of liver injury. In addition, tissue replacement by endogenous cells (i.e., regeneration) must be distinguished from reconstitution by transplanted donor cells...

Yet cultural meanings are also local and contested. This aspect of culture highlights its dynamic, changing quality and gives weight to forces of change and interaction. From this perspective, culture is constantly being transformed. People within groups may be aware of group norms, but those norms themselves change over time, and people choose to reject the norms or manipulate their behavior within them. For example, human beauty standards, and their health-related consequences, change dramatically over time. The corset allowed one set of health problems (muscle atrophy, liver damage) to emerge, whereas a century later breast augmentation caused others (pain, scar tissue, implant rupture). Food preferences, time pressure, and large-scale industrial meal production combine to create a new epidemic of obesity based on fast food and sedentism.

At increased risk of developing the clinical outcome that investigators are trying to prevent. For example, in a lipid lowering trial with all cause mortality as the primary outcome, patients with an increased risk of dying from reasons unrelated to lipids lipoproteins are excluded. This would, for example, apply to those with cancer or serious kidney or liver damage who can be expected to have shortened life expectancy. Inclusion of patients who are dying from other conditions during a trial will add background noise to the trial findings by diluting any mortality effect of the new lipid lowering agent. Thus, the ability to ascertain the true effect of an intervention is lessened in the presence of competing risk.

Today, the most high-risk group for development of pellagra signs and symptoms in Western society is chronic alcoholics, whose diets are often poor, and in addition are subject to liver damage from alcohol abuse and its cellular toxicity. Certain forms of psychosis, including depression and schizophrenia, are associated with abnormalities of the tryptophan metabolism pathways, including those involved in the formation of 5-hydroxytryptamine (serotonin)

Or bacteria-induced TNF release, liver damage, NO production, mortality, and protected against cardiovascular depression (81). In healthy volunteers, BPI causes a significant reduction in serum LPS, TNF, IL-6, IL-8, IL-10 levels, and several other parameters (82). The results of a clinical study in children with meningococcal sepsis were promising of the 26 patients, only 1 died (4 ) (83). However, in a larger placebo-controlled study, the mortality in the rBPI21-treated patients was not significantly reduced, although there was a trend towards improved outcome in the primary outcome variables (84). The feasibility of the use of BPI for the treatment of sepsis and septic shock in humans may be restricted due to the limited halflife of approximately 10 minutes in vivo (85).

Choline, methionine, methyltetrahydrofolate (methyl-THF), and vitamins B6 and B12 are closely interconnected at the transmethylation metabolic pathways that form methionine from homocys-teine. Perturbing the metabolism of one of these pathways results in compensatory changes in the others. For example, as noted above, choline can be synthesized de novo using methyl groups derived from methionine (via S-adenosylmethio-nine). Methionine can be formed from homocys-teine using methyl groups from methyl-THF, or using methyl groups from betaine that are derived from choline. Similarly, methyl-THF can be formed from one-carbon units derived from serine or from the methyl groups of choline via dimethylglycine. When animals and humans are deprived of choline, they use more methyl-THF to remethylate homocysteine in the liver and increase dietary folate requirements. Conversely, when they are deprived of folate, they use more methyl groups from choline, increasing the dietary requirement for...

Treatment of heart failure is directed to correction of the two major problems associated with failure venous congestion and reduced cardiac output. Systemic venous congestion can cause renal and liver damage as well as discomfort. The threat of pulmonary edema from pulmonary congestion has already been discussed. Diuretics and reduced salt intake can reduce the accumulated blood volume and venous congestion even though these treatments may actually lower the filling pressure of the heart and thus the stroke volume. One of the oldest cardiac drugs is digitalis, which increases the contractility of the heart by causing the muscle cells to accumulate SR calcium (see Chapter 11). Increasing contractility with digitalis increases the cardiac output and lowers the venous pressure. Digitalis in the absence of a diuretic will often cause a brisk diuresis, as the kidney detects the rising cardiac output. Although digitalis and other cardiac stimulants can improve the exercise tolerance in...

After the systemic administration of adenoviral vectors, most of the virus ends up in the liver. When adenoviral replication is not strictly restricted to certain cell types or tissues, severe liver damage might occur due to adenoviral replication and consequential lysis of the liver cells. Because of this importance to restrict adenoviral replication, solutions have to be found for the observed aspecific replication of CRAds. One solution is a double-controlled conditionally replicating adenovirus (dcCRAd). 8 In a dcCRAd not one but two replication essential genes are controlled by two tumor-specific promoters. For example, both the adenoviral E1A and E1B genes have been placed under the control of two different tumor-specific promoters. Also, studies have already been conducted with both the E1A and the E4 gene under control of two different tumor-specific promoters.1-9-1 E1A, E1B, and E4 are all examples of adenoviral genes that are essential for replication of the adenovirus. The...

Methotrexate is normally well tolerated, although nausea is common and can cause patients to stop therapy. Acute myelosuppression is a more important cause of serious morbidity and mortality than the chronic liver damage for which methotrexate is well recognised.

The second-generation intercalator-like PARG inhibitors are ideal for in vivo studies due to their low molecular weights and good cell permeability properties. One member of the Tilorone family of PARG inhibitors, GPI 16552 or 2,7-bis has exhibited neuroprotec-tive properties in a rat model of focal cerebral ischemia. Both a 30-minute pre-ischemia treatment or a 1- or 2-hour post-ischemia treatment with GPI 16552 reduces the total infarct volume by 47-53 , with greater protection observed in the cortical areas (43-59 ) than in the subcortical areas (28-40 ) of the brain (Lu et al., 2003). Furthermore, application of the novel PARG inhibitor GPI 18214 substantially reduces the septic-shock-like syndrome caused by zymosan in mice (Genovese et al., 2004). Zymosan is a nonbacterial, nonendotoxic agent that produces liver, intestine, lung, and kidney failure in test animals. In mice treated with 40 mg kg of GPI 18214, which has an IC50 value of 3.0 mM, all signs of pancreatic, renal, and...

The two concerns about aflatoxins are their acute toxicity and ability to produce cancer. The LD50 of aflatoxin is 0.5 mg kg of the body weight, and death occurs within 72 h. Death is due to liver damage and hemorrhaging in the intestinal tract and peritoneal cavity. As animals mature, they become more resistant. Compared with a substance such as lead whose toxicity is about 500 mg kg of body weight, aflatoxin is extremely toxic. Consumption of aflatoxin at sublethal concentration for several days to several weeks results in moderate to severe liver damage. Several forms of hepatic damage include biliary hyperplasia or excessive growth of cells in the bile duct region of the liver. Also prevalent are accumulation of fat and changes in appearance of the liver from purple-red to yellow-red.

Nucleic acids are a necessary component of all cells, and are found in relatively high levels in rapidly dividing cells. Thus, the nucleic acid content of yeast (around 10 of dry weight) is approximately five times greater than in the average mammalian organ. When nucleic acids are ingested, they are first attacked in the duodenum by pancreatic nuclease. The resulting nucleotides are then attacked by nucleotidases in the intestine, resulting in nucleosides and phosphate. These in turn are further degraded to purine and pyrimidine bases. The degradation of purine bases in man results in the production of uric acid. Accumulation of uric acid beyond the excretion capacity of the kidney results in the formation of crystalline deposits in the joints and soft tissues, leading to goutlike manifestations and calculi in the urinary tract. Pyrimidines are degraded to orotic acid, the accumulation of which results in liver damage. The administration of foods of microbial origin is limited by the...

Surrogate outcomes have a smaller sample size than conventional morbidity mortality studies, so the available information regarding intervention safety is compromised. There are few good surrogate markers of drug safety. Increases in liver function tests predict liver damage or failure and QT prolongation on the electrocardiogram is associated with higher risks of serious ventricular arrhythmias and sudden cardiac death.

Fig. 1 Potential pathways of nonesterified fatty acid (NEFA) metabolism in liver. In conditions of undernutrition, fat is mobilized from adipose tissue, resulting in increased NEFA concentration in plasma and increased NEFA uptake by liver. In ketosis, there is an increase in the proportion of acetyl CoA converted to ketone bodies. Fatty liver arises as the formation of triacylglycerols from NEFA increases without a corresponding increase in secretion of very low density lipoproteins (VLDL). Fig. 1 Potential pathways of nonesterified fatty acid (NEFA) metabolism in liver. In conditions of undernutrition, fat is mobilized from adipose tissue, resulting in increased NEFA concentration in plasma and increased NEFA uptake by liver. In ketosis, there is an increase in the proportion of acetyl CoA converted to ketone bodies. Fatty liver arises as the formation of triacylglycerols from NEFA increases without a corresponding increase in secretion of very low density lipoproteins (VLDL).

Hepatobiliary complications, including steatosis and cholestasis, are associated with PN patients due to the lack of enteral stimulation and limited gastrointestinal motility. Cholestasis is universal in patients receiving PN for more than 6 weeks without enteral feedings. Transition to enteral or oral feedings will help prevent the potential development of gallstones associated with cholestasis. In adults, hepatic steatosis, or fatty liver, is generally

The adipose fat cell is not only a passive storage site but an endocrinologically active secretor of many substances like leptin, adiponectin, and cyto-kines, which participate in an inflammatory response and may mediate a host of adverse consequences, including insulin resistance and diabetes. Obesity is related to an increased risk of developing type 2 insulin-resistance diabetes mellitus, hyper-lipidemia, heart disease, obstructive sleep apnea, asthma and other respiratory problems, back pain and orthopedic problems, fatty liver (nonalcoholic steato-hepatitis or NASH), gallstones, and depression. The increasing incidence of type 2 diabetes in obese adolescents is already being noticed, with estimates of 200 000 diabetics under age 20 years in the US predicted to rise to a lifetime risk of developing diabetes of 33-39 for those born in the year 2000.

Hepatitis B, or serum hepatitis, is spread mainly through contaminated blood, often from unsterilized needles shared by drug users or used for tattoos or ear or body piercing. The virus can also be transmitted sexually. Over 100,000 people are infected yearly in the United States, but this number is decreasing due to the recent introduction of a vaccine. In addition to the initial disease, which is more severe than hepatitis A (more liver damage and fatality rate of 10 ), those infected are at higher risk of liver cancer.

In addition to its myeloablative effects, HDC is extremely toxic to other tissues with dividing cells, such as the gastrointestinal tract, the skin, and the hair follicles. Acute toxicities include cramping and dysfunction in the gastrointestinal tract, mouth sores, nausea, diarrhea, rashes, and fatigue. Total hair loss is very common but varies with the type of chemotherapy used. Severe organ toxicity is less common but can be fatal. The lungs are particularly sensitive to some drugs (e.g., vincristine in the Solid Tumor Autologous Marrow Program I regimen), and life-threatening interstitial pneumonitis can occur, resulting in fluid accumulation and reduced blood oxygen. Other severe adverse effects may include liver damage and inflammation of the bladder. Cardiac events occur more often with HDC. For these reasons, patients who underwent HDC ABMT were usually hospitalized for several weeks and sometimes for months if complications occurred. During hospitalization, patients were at...

Hepatic disease Abnormalities in hepatic function are commonly reported in obese people. Fatty liver, due to increased concentrations of fatty acids, digly-cerides, and triglycerides in hepatocytes, is reported in obese people. The frequency of fatty liver has been reported to be as high as 94 in very obese subjects. A small number of very obese subjects will develop micronodular cirrhosis. Abnormal liver enzymes on laboratory screening are very common in obese people and do not require further evaluation unless they are markedly elevated. Weight loss results in disappearance of the excess fat and normalization of the liver function tests.

Breathing air with very high levels of cadmium severely damages the lungs and can cause death. Breathing lower levels for years leads to a build-up of cadmium in the kidneys, which can cause kidney disease. Long-term oral exposure to cadmium leads to nephrotoxicity. Renal effects always occur before or with other effects. Other effects that may occur after breathing cadmium for a long time are lung damage and fragile bones. Workers who inhale cadmium for a long time may have an increased chance of getting lung cancer. There is no proof about mice or hamsters getting lung cancer on breathing cadmium. However, some rats that breathe cadmium develop lung cancer. In humans, breathing cadmium can affect the ability to have children or can harm unborn babies. Female rats and mice that breathe high levels of cadmium have fewer litters and the pups may have more birth defects than usual. Breathing cadmium causes liver damage and changes in the immune systems of rats and mice. Eating food or...

Fumonisin B1 was identified as an etiological agent responsible for ELEM in horses and other Equidae (donkeys and ponies) and for porcine pulmonary edema (PPE) Jackson et al. 1996 reviewed in Summerell et al. (2001) . ELEM is characterized primarily by neurotoxic effects, including uncoordinated movements and apparent blindness showing as violent blundering into stalls and walls. The levels of FmB1 and FmB2 in feeds associated with confirmed cases of ELEM ranged from 1.3 to 27 ppm. In pigs, PPE occurs only at high FmB levels (175 ppm), while liver damage occurs at much lower concentrations with a NOAEL of &lt 12 ppm. FmB1 resulting in left-sided heart failure alters cardiovascular function. In the cattle, renal injury, hepatic lesions, and alteration of sphingolipid in various organs was observed (Haschek et al. 2001). Similar to AAL toxin, Fms are also

Acute hepatitis A is not distinguishable from other forms of viral hepatitis on clinical grounds, although the diagnosis may be inferred in a patient with typical symptoms and the appropriate epidemiologic clues. Liver function tests, especially serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), are sensitive measures of parenchymal liver damage, but are not specific for hepatitis A.

A wide variety of feed toxins specifically attack the liver. Usual symptoms of liver damage such as jaundice (or, icterus) and elevated liver enzymes in the blood may be present, but usually the first symptoms noticed are severe damage to the skin on exposure to sunlight. Liver damage can become fairly advanced before stock owners notice their animals are behaving as if they are ill, so blood may not be drawn or the color of membranes assessed in the early stages. But when the liver has been damaged, chlorophyll and related plant pigments cannot be completely catabolized, and some of the intermediate breakdown products build up in the blood. These fragments capture energy from sunlight and release it in such a way that overlying skin tissue is damaged and may develop into serious sores, sloughing off and leaving the animal open to infection. This secondary photosensitiza-tion is observed after liver damage caused by the ingestion of pyrrolizadine alkaloids from groundsel (Senecio),...

Overfeeding usually results from overestimation of caloric needs. Overestimation occurs when actual body weight is used, such as in critically ill patients with significant fluid overload and in obese patients. Indirect calorimetry can be used to quantify energy requirements. Estimated dry weight should be obtained from preinjury records or family members. Adjusted lean body weight can also be calculated. Clinically, increased oxygen consumption, increased carbon dioxide production, fatty liver, suppression of leukocyte function, and increased infectious risks have been documented with overfeeding.

Aflatoxins are produced by molds growing in corn, peanuts, and other grain and pulse crops. This widespread toxicant can cause reduced feed intake and both acute and chronic liver damage. Highly carcinogenic, this is one of the few important natural toxins that can pass into animal products in sufficient amounts to threaten human health. Zearalenone, which is produced by a different mold in corn, is a powerful estrogen analogue that can cause feminization of male animals and disruption of reproduction in females.

Chronic alcoholic patients are often iron deficient because of increased frequency of gastrointestinal bleeding, typically due to alcoholic gastritis or eso-phageal tears from frequent retching and vomiting, or from rupture of esophageal varices in patients with cirrhosis and portal hypertension. The major consequence of iron deficiency is anemia, which may be compounded by the concurrent effects of folate and pyridoxine deficiencies. Conversely, increased exposure to iron, e.g., from cooking in iron pots, increases the likelihood and severity of alcoholic liver disease, since the presence of iron in the liver promotes oxidative liver damage during the metabolism of alcohol.